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Both mechanisms of telomere length maintenance, telomerase and ALT activity, are known to co-exist in cancer cells (De Vitis et al 2018

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in the tissues, O 2 is unloaded from Hb that undergoes a spatial rearrangement of the globin chains, allowing the entry of 2,3-diphosphoglycerate (2,3-DPG) which diminishes O 2 affinity [1, 2]